From
YAHOO! NEWS. Monday
Aprill 17, 7:31pm
EVASIVE ACTION
BY
NELL
BOYCE
A DRUG designed thirty years ago to treat multiple
sclerosis might suppress a whole range of autoimmune diseases. It produces a
shift in the immune system that counteracts the way the body turns on itself,
say researchers in the US.
The body can mount two distinct types of
immune response: Th1 orTH2. The two are antagonistic—signals that stimulate
one inhibit the other and vice versa. In multiple sclerosis, an inflammatory,
Th1-type response destroys proteins in the myelin sheath that covers nerves.
In 1967, researchers in Israel synthesized a drug made from amino acids found in
myelin basic protein. The drug, glatiramer acetate (GA), seemed to protect the
nerves of animals with MS-like diseases, presumably by attracting immune system
cells that would otherwise attack
myelin. Patients given the drug also had fewer relapses.
But now David Hafler at Harvard Medical School and his team have evidence that
the drug alters the immune system
in a more general way. They analysed T-cell lines from MS patients before and
after a long course of GA treatment, and then looked at how these cells
responded to antigens such as myelin basic protein, GA itself, and other
proteins and peptides associated with autoimmune disease.
After treatment with GA, T cells are more likely to cross-react with many
different peptides. Crucially, they also released Th2 cytokines: signals that
should elicit aTh2 response and counteract the Th1 response to the peptides
involved in MS.
“It was previously thought it worked by looking like the myelin proteins, “
Hafler says. But it “kind of
looks like everything”, because
it is a random arrangement of four amino acids created before scientists knew
precisely how to generate a desired protein. Beause GA stimulates a shift away
from the damaging Th1 respone, Hafler believses that it could be useful for
treating autoimmune diseases caused by other antigens. Hafler points out that
Igal Gery at the National Institutes of Health near Washington DC recently found
that the drug protects mice against
an autoimmune eye disease called uveoretinitis.
Roland Martin, of the National Institute of Neurological Disorders and Stroke
near Washington DC, has completed a similar but unpublished study of how GA
affects T cells. He says that it would be difficult to prove that the shift to
Th2 is truly the mechanism behind GA`s effectiveness against
multiple sclerosis. But he agrees that the theory makes sense.
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